ECG Challenge: Rushing to the ED With Chest Pain

Philip J. Podrid, MD

Disclosures

March 21, 2022

The correct diagnosis is sinus rhythm, right bundle branch block (RBBB), left anterior fascicular block, and acute STEMI (Figure 2).

Figure 2.

Discussion

The rhythm is regular with a rate of 90 beats/min, although there is one premature complex (*). A P wave precedes each QRS complex (+) with a stable PR interval of 0.18 sec. The P waves are positive in leads I, II, aVF, and V4-V6; this is a normal sinus rhythm.

The QRS complexes are wide (0.14 sec) and have the morphology of an RBBB with an RSR' morphology in V1 (→) and a broad S wave in leads I and V5-V6 (←). The axis is extremely leftward with a positive QRS complex in lead I and a negative complex in leads II and aVF. This axis may represent either an old MI in which there are deep Q waves in leads II and aVF, or a left anterior fascicular block in which an initial R wave occurs in these leads, as seen here. Therefore, this is a left anterior fascicular block. Along with the RBBB, this is termed bifascicular block or disease.

The T waves in leads V2-V5 are abnormal. While they are not tall and peaked, they are symmetric(┴), termed hyperacute T waves consistent with hyperkalemia localized to the anterior wall. There is no J-point elevation but the ST segment is shortened (^). These features are the earliest changes seen with an acute transmural MI, especially given the clinical history, and they occur prior to ST segment elevation — called an early acute transmural MI of the anterior wall.

With an acute occlusion of a coronary artery and transmural ischemia:

  • ATP breaks down to adenosine and is not resynthesized because this energy-dependent process requires oxygen.

  • Membranes lose integrity, normally maintained by a sodium-potassium ATPase-dependent pump that moves potassium into the cell (resulting in high intracellular potassium) and sodium out (resulting in low intracellular sodium). The high intracellular and low extracellular potassium is necessary to maintain the normal resting membrane potential of -90 mv which is important for the normal rapid upstroke of phase 0 of the action potential which determines membrane conduction velocity.

  • Potassium leaks out and sodium leaks in according to an intracellular-extracellular gradient, resulting in localized elevations in potassium levels.

  • The inward leak of sodium activates a sodium-calcium exchanger that is energy- and oxygen-independent.

The intracellular hypercalcemia shortens the ST segment. Because there is no blood flow in or out of the area of the infarction, the high potassium levels persist, causing localized hyperkalemia and hyperacute T waves. The J-point and ST elevations occur afterward.

The absence of blood flow in and out of the area also means that the cardiac biomarkers will not wash out into the systemic bloodstream, accounting for a delay in seeing elevated levels.

Philip Podrid, MD, is an electrophysiologist, a professor of medicine and pharmacology at Boston University School of Medicine, and a lecturer in medicine at Harvard Medical School. Although retired from clinical practice, he continues to teach clinical cardiology and especially ECGs to medical students, house staff, and cardiology fellows at many major teaching hospitals in Massachusetts. In his limited free time he enjoys photography, music, and reading.

You can follow Dr Podrid on Twitter @PPodrid

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